CANCER GENETICS
Bcb29-003	A Pan-Cancer Multi-Omic Analysis of Copy Number Signature Clusters and Genomic Instability
	Quote:	Feature importance analysis highlighted expression-driven predictors and pathways linked to genomic instability. These findings show that current CNS frameworks capture complementary rather than interchangeable dimensions of tumor genome instability and suggest that multi-omic profiles can extend signature-based stratification to cohorts without whole-genome sequencing.
	Article:	https://www.biorxiv.org/content/10.64898/2026.07.20.739333v1
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	Search Authors:	Marco Rota Negroni Ilaria Billato Chiara Romualdi,
GENETICS
Bgn29-006	Comprehensive landscape of potential CTCF-binding sites across the complete telomere-to-telomere human genome
	Quote:	CCCTC-binding factor (CTCF) is a master regulator of the human genome, directly modulating both transcription and 3D genome organization. However, previous human genome-wide maps of its binding sites have been built on an incomplete assembly, leaving out many repetitive, difficult-to-sequence regions.... Subterminal heterochromatin spacer regions contain CTCF sites deriving largely from ancient LINE elements and lineage-specific segmental duplications act as a site transfer mechanism between species. We believe that our findings will provide the foundation for future studies of CTCFs function in the repetitive parts of the human genome.
	Article:	https://www.biorxiv.org/content/10.64898/2026.07.18.739380v1
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	Search Authors:	Eleftherios Bochalis Ilias Georgakopoulos-Soares,
GENETICS
Bgn29-011	Architectural chromatin interactions provide a framework for context-dependent gene regulation
	Quote:	Genes connected to these dual-state regulatory elements are enriched for developmental and signaling pathways and exhibit increased expression specificity across cell types, consistent with specialized roles in context-dependent gene regulation. Together, our findings provide a biologically informed framework for classifying and interpreting chromatin interactions and.,..
	Article:	https://www.biorxiv.org/content/10.64898/2026.07.17.739237v1
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	Search Authors:	Mary Likhite Gregory R Andrews Mingshi Gao Vivekanandan Ramalingam Vivian Hecht Anshul Kundaje Jill E Moore,
PRIME AGING BRAIN GENETICS
Mne29-009	Epigenetic Clock Trajectories and Brain Health in Midlife
	Quote:	Accelerated biological aging can be assessed with DNA methylation (DNAm)-based epigenetic clocks. Research suggests that greater DNAm is associated with faster cognitive decline and risk of Alzheimer disease (AD) and other dementias. ,,, Conclusion Middle-aged adults with faster 15-year epigenetic aging trajectories demonstrated worse cognitive performance, whereas those with slower biological aging trajectories exhibited cognitive resilience and more favorable AD biomarker profiles. By examining long-term trajectories rather than single timepoints, these findings identify individuals at differential risk for brain health outcomes.
	Abstract:	https://www.medrxiv.org/content/10.64898/2026.07.16.26358251v1
	Full Text:	https://www.medrxiv.org/content/10.64898/2026.07.16.26358251v1.full-text
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	Search Authors:	Ana I. Boeriu Shea J. Andrews Tina Hoang Sejong Bae Kristine Yaffe,

Javilk's Research Links Newsletter for Week 29
Updated 07/25/2026-03:15:16 AM
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Bcb29-003

A Pan-Cancer Multi-Omic Analysis of Copy Number Signature Clusters and Genomic Instability

Bgn29-006

Comprehensive landscape of potential CTCF-binding sites across the complete telomere-to-telomere human genome

Bgn29-011

Architectural chromatin interactions provide a framework for context-dependent gene regulation

Mne29-009

Epigenetic Clock Trajectories and Brain Health in Midlife